Osophagus and stomach

Question 1

State the basic plan of the gut wall from the lumen outwards.

Answer 1

Epithelium, lamina propria, submucosa, muscularis, serosa/adventitia

There are nerve plexuses in the submucosa and muscularis

Serosa is a mixture of connective tissue and epithelium

Adventitia is only connective tissue

Question 2

What vertebral level does the oesophagus start at?

Answer 2

C5

Question 3

How long is the average oesophagus?

Answer 3

25-30cm

Question 4

At what vertebral level does the oesophagus pierce the diaphragm?

Answer 4

T10

Question 5

Describe the cell type in the upper oesophagus and the reason for having this cell type.

Answer 5

Non-keratinising stratified squamous - this is good for protection - acts as a barrier and prevents the loss of water through the epithelium

Question 6

What are the two important sphincters in the oesophagus?

Answer 6

Upper oesophageal sphincter and the lower oesophageal sphincter

Question 7

Describe the difference in structure of the lower and upper oesophageal sphincters.

Answer 7

The upper oesophageal sphincter is made up of only skeletal muscle whereas the lower oesophageal sphincter consists of both skeletal and smooth muscle.

Question 8

What state are the sphincters in when there is no food in the mouth?

Answer 8

They are tonically active meaning that they are both closed.

Question 9

What happens when food goes into the mouth?

Answer 9

When food goes into the mouth, a reflex is set up by the swallowing centre in the brain leading to peristalsis.

Question 10

How does muscle type change as you pass down the oesophagus?

Answer 10

You go from skeletal to smooth muscle as you move down the oesophagus.

Question 11

How does the innervation change as you pass down the oesophagus?

Answer 11

It goes from motor neurones to autonomic nervous system as you move down the oesophagus.

Question 12

What two types of muscle are in the oesophagus?

Answer 12

Circular and longitudinal

Question 13

What is the difference between the primary and secondary peristaltic waves?

Answer 13

Secondary peristaltic wave is initiated after the primary if the food gets stuck.

Question 14

The lower oesophageal sphincter is not considered a true anatomical sphincter. What is it formed by?

Answer 14

Diaphragm (muscular part), greater curvature of the stomach folding inwards, difference in pressure between the thorax and abdomen

Question 15

What are the gastric folds in the stomach lining called and what is the point in them?

Answer 15

Rugae - they increase surface area and allowing folding of stomach when empty

Question 16

Describe the transition in epithelium from the oesophagus to the stomach.

Answer 16

Oesophagus is made up of non-keratinising stratified squamous epithelia and the stomach epithelium is made up of simple columnar epithelium

Question 17

What are the 4/5 regions of the stomach?

Answer 17

Cardiac, Fundus, Body, Pylorus and Pyloric Antrum

Question 18

Certain substances are produced in certain regions of the stomach. State which substances are produced in which regions.

Answer 18

Cardiac and Pyloric regions - mucus only

Fundus and Body - pepsinogen, HCl, mucus

Antrum - gastrin

Question 19

What feature do the mucus secreting cells of the stomach have that protects them from the acidity of the stomach?

Answer 19

They secrete HCO3- that sits on top of these cells and neutralises the acid that comes into contact with its surface

Question 20

How much acid is produced by the stomach per day and what is the concentration of protons?

Answer 20

2 L

150 mM

Question 21

What do Gastric Chief Cells produce?

Answer 21

Gastric Chief Cells produce pepsinogen

Question 22

State some histological features of Gastric Chief Cells.

Answer 22

They have a lot of RER

They have Golgi apparatus for packaging and modifying for export

They have a lot of vesicles at the apical membrane

Question 23

State three structural features of the resting parietal cell.

Answer 23

Numerous mitochondria - provide energy for the active transport of protons into the lumen of the stomach

Cytoplasmic Tubulovesicles - contain H+/K+ ATPase channels

Internal Canaliculi - fluid filled reservoirs present within the resting parietal cell

Question 24

What is the role of parietal cells?

Answer 24

Parietal cells pump protons into the lumen of the stomach and make it more acidic

Question 25

Describe the mechanism by which active parietal cells increase the proton concentration in the stomach.

Answer 25

Carbon dioxide diffuses into the cell from the blood and reacts with water with the action of carbonic anhydrase to produce bicarbonate and a proton. A sodium-potassium exchanger bring one potassium in and one sodium out. The K+ follows the concentration gradient and diffuses into the canaliculi. HCO3- is exchanged for Cl- - the Cl- then moves down the concentration gradient into the canaliculi. Then, ATP is used to actively transport H+ into the canaliculi with K+ moving out. There is a massive ATP driven movement of protons into the stomach lumen.

Question 26

What is the effect of inhibiting carbonic anhydrase?

Answer 26

This reduces the acid producing ability of the parietal cells because it is no longer able to convert water and carbon dioxide into H2CO3 (so H+ and HCO3- isn’t generated)

Question 27

What two proteins do you need a lot of to increase the acidity of the stomach?

Answer 27

Carbonic Anhydrase and H+/K+ ATPase

Question 28

How does pepsinogen turn into pepsin?

Answer 28

The acid makes the pepsinogen unfold and this causes autocatalysis (pepsinogen metabolises itself) of pepsinogen to produce pepsin.

Question 29

What are the two stimuli for gastrin production?

Answer 29

Acid production itself

Local peptide hormones that are being produced by pepsin

Question 30

What is the effect of gastrin?

Answer 30

Gastrin is produced in the pyloric antrum and passes into the bloodstream before returning to the lumen of the stomach where it causes an increase in acid secretion by the stomach epithelium.

Question 31

How can gastrin indirectly increase acid secretion?

Answer 31

Gastrin stimulates the release of histamine from chromaffin cells (in the lamina propria) - this stimulates acid secretion

Question 32

What are the three phases of gastric secretion?

Answer 32

Cephalic, Gastric, Intestinal

Question 33

Describe the cephalic phase of gastric secretion.

Answer 33

This is before the food even enters your mouth. The vagus nerve from the medulla stimulates the enteric nervous system to increase the production of acid and pepsin. You also get an increase in gastrin production (which causes further increase in acid production).

Question 34

Describe the gastric phase of gastric secretion.

Answer 34

Once the food is in the stomach, stretch and chemoreceptors send messages to the brain. The brain then activates the vagus nerve and increases pepsin and acid production. Once the process has been started, the enteric nervous system will take over and cause churning of the stomach.

Question 35

Describe the intestinal phase of gastric secretion.

Answer 35

Chyme enters the small intestine and if the pH is < 2 or the chyme has a high lipid content, this acts as a stimulus that goes up to the brain and switches off acid and pepsin production.

Question 36

What are the three hormones produced in the enterogastric reflex? What is the name given to this group of hormones?

Answer 36

Gastric Inhibitory Peptide, Cholecystokinin and Secretin

These are enterogastromes

They decrease the production of acid and pepsin

The enterogastric reflex is a reflex that is controlled by hormones

Question 37

Describe the excitatory process when chyme has a high protein content.

Answer 37

If the chyme entering the small intestine has a high protein content it will stimulate the release of gastrin so that more acid is produced hence more pepsinogen is converted to pepsin so the proteins will be better digested.

Question 38

State two drugs that decrease acid secretion and their targets.

Answer 38

Omeprazole - proton pump inhibitor

Ranitidine - histamine receptor antagonist